Background: The previous study investigated whether the functions of small, medium, and large high density lipoprotein (S/M/L-HDL) are correlated with protein changes in mice. Herein, the proteomic and functional analyses of high density lipoprotein (HDL) subclasses were performed in humans and rats.
Methods: After purifying S/M/L-HDL subclasses from healthy humans (n = 6) and rats (n = 3) using fast protein liquid chromatography (FPLC) with calcium silica hydrate (CSH) resin, the proteomic analysis by mass spectrometry was conducted, as well as the capacities of cholesterol efflux and antioxidation was measured.
Although elevation of HDL-C levels by pharmaceutical drugs have no benefit of cardiovascular endpoint, the effect of high-density lipoprotein/apolipoprotein A1 (HDL/apoA-1) replacement therapy on atherosclerosis is controversial. The current meta-analysis analyzed the effects of HDL/apoA-1 replacement therapies on atherosclerotic lesions both in humans and mice. The PubMed, Cochrane Library, Web of Science, and EMBASE databases were searched through June 6, 2020.
View Article and Find Full Text PDFBackground: High levels of lipoprotein(a) (Lp(a)) is an independent risk factor for premature coronary heart disease (PCHD). It is also considered a residual risk for controlled low density lipoprotein cholesterol (LDL-C). Dietary control, exercise, and drugs have limited effects on the levels of Lp(a).
View Article and Find Full Text PDFBackground: This study investigated whether combinations of high-density lipoprotein (HDL) subfractions and inflammatory markers would add value to coronary artery disease (CAD) prediction.
Methods: Non-CAD subjects (n=245) were stratified into low/moderate/high-Framingham risk (L/M/H-FR) groups and 180 CAD patients were enrolled. Levels of HDL-C, HDL, HDL, monocyte chemoattractant protein-1 (MCP-1), and high-sensitivity C-reactive protein (hsCRP) were measured.
Purpose: Intracellular cholesterol imbalance plays an important role in adipocyte dysfunction of obesity. However, it is unclear whether obesity induced monocyte chemoattractant protein-1 (MCP-1) causes the adipocyte cholesterol imbalance. In this study, we hypothesize that MCP-1 impairs cholesterol efflux of adipocytes to HDL2 and insulin rescues this process.
View Article and Find Full Text PDFBackground: Type A acute aortic dissection (TA-AAD) has high mortality, with 50% of patients dying before hospital admission. Hypertension is the most common comorbidity for acute aortic dissection, and effective antihypertensive therapy is still unable to predict the risk of aortic rupture at the medium- and long-term stages. While the presence of renal cyst has been found to increases the risk of thoracic aortic disease, the correlation between renal cyst and TA-AAD with hypertension remains poorly understood.
View Article and Find Full Text PDFHypertrophic cardiomyopathy (HCM), the most common heritable cardiomyopathy, is associated with a high risk of sudden cardiac death. The complexity and behavior of the circular RNA (circRNA)-associated competing endogenous RNA (ceRNA) network in HCM have not been thoroughly elucidated. Plasma circRNA and messenger RNA (mRNA) expression profiles were acquired by using a microarray.
View Article and Find Full Text PDFHigh density lipoprotein (HDL) has been proposed to be internalized and to promote reverse cholesterol transport in endothelial cells (ECs). However, the mechanism underlying these processes has not been studied. In this study, we aim to characterize HDL internalization and cholesterol efflux in ECs and regulatory mechanisms.
View Article and Find Full Text PDFMonocyte chemoattractant protein-1 (MCP-1) plays crucial roles at multiple stages of atherosclerosis. We hypothesized that MCP-1 might impair the reverse cholesterol transport (RCT) capacity of HepG2 cells by decreasing the cell-surface protein expression of ATP binding cassette A1 (ABCA1), ATP binding cassette G1 (ABCG1), and scavenger receptor class B type I (SR-BI). MCP-1 reduced the total protein and mRNA levels of ABCA1 and SR-BI, but not of ABCG1.
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